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功能性中央多聚嘌呤序列为1型人类免疫缺陷病毒基因组提供下游保护,使其免受载脂蛋白B mRNA编辑酶催化多肽样蛋白3G(APOBEC3G)和载脂蛋白B mRNA编辑酶催化多肽样蛋白3B(APOBEC3B)的编辑。

Functional central polypurine tract provides downstream protection of the human immunodeficiency virus type 1 genome from editing by APOBEC3G and APOBEC3B.

作者信息

Wurtzer Sebastien, Goubard Armelle, Mammano Fabrizio, Saragosti Sentob, Lecossier Denise, Hance Allan J, Clavel François

机构信息

Unité de Recherche Antivirale, INSERM U552, Paris, France.

出版信息

J Virol. 2006 Apr;80(7):3679-83. doi: 10.1128/JVI.80.7.3679-3683.2006.

Abstract

Lentiviruses utilize two polypurine tracts for initiation of plus-strand viral DNA synthesis. We have examined to what extent human immunodeficiency virus type 1 plus-strand initiation at the central polypurine tract (cPPT) could protect the viral genome from DNA editing by APOBEC3G and APOBEC3B. The presence of a functional cPPT, but not of a mutated cPPT, extensively reduced editing by both APOBEC3G and APOBEC3B of sequences downstream, but not upstream, of the cPPT, with significant protection observed as far as 400 bp downstream. Thus, in addition to other potential functions, the cPPT could help protect lentiviruses from editing by cytidine deaminases of the APOBEC family.

摘要

慢病毒利用两个多聚嘌呤序列来起始正链病毒DNA的合成。我们已经研究了人类免疫缺陷病毒1型在中央多聚嘌呤序列(cPPT)处的正链起始在多大程度上能够保护病毒基因组免受载脂蛋白B mRNA编辑酶催化多肽样3G(APOBEC3G)和载脂蛋白B mRNA编辑酶催化多肽样3B(APOBEC3B)的DNA编辑。功能性cPPT的存在,而非突变型cPPT的存在,能显著减少cPPT下游(而非上游)序列被APOBEC3G和APOBEC3B编辑的程度,在下游400 bp处仍观察到显著的保护作用。因此,除了其他潜在功能外,cPPT可能有助于保护慢病毒免受APOBEC家族胞嘧啶脱氨酶的编辑。

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